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Protein Cell. 2014 Jul;5(7):503-17. doi: 10.1007/s13238-014-0058-8. Epub 2014 Apr 23.

The regulation of TGF-β/SMAD signaling by protein deubiquitination.

Author information

1
Life Sciences Institute, Zhejiang University, Hangzhou, 310058, China.

Abstract

Transforming growth factor-β (TGF-β) members are key cytokines that control embryogenesis and tissue homeostasis via transmembrane TGF-β type II (TβR II) and type I (TβRI) and serine/threonine kinases receptors. Aberrant activation of TGF-β signaling leads to diseases, including cancer. In advanced cancer, the TGF-β/SMAD pathway can act as an oncogenic factor driving tumor cell invasion and metastasis, and thus is considered to be a therapeutic target. The activity of TGF-β/SMAD pathway is known to be regulated by ubiquitination at multiple levels. As ubiquitination is reversible, emerging studies have uncovered key roles for ubiquitin-removals on TGF-β signaling components by deubiquitinating enzymes (DUBs). In this paper, we summarize the latest findings on the DUBs that control the activity of the TGF-β signaling pathway. The regulatory roles of these DUBs as a driving force for cancer progression as well as their underlying working mechanisms are also discussed.

PMID:
24756567
PMCID:
PMC4085288
DOI:
10.1007/s13238-014-0058-8
[Indexed for MEDLINE]
Free PMC Article

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